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This article shows a correlation between certain genetic markers and educational attainment. While there might be a correlation, I think it would be tempting certain people who would push a racist agenda instead of objectively analyzing data or performing more in-depth research as opposed to revisiting "The Bell Curve" or eugenics research from 100 years ago. Still it's interesting to think that my sitting in a college classroom is the result of certain genetic markers.

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A study released today has found that an individual's genetic makeup can have a direct effect on the level of education achieved by that individual, the first time that researchers have found such a relationship. And while the impact is found to be relatively small compared to other external factors, the researchers say it's still significant enough to consider.

This new study, published in AERA Open, a journal of the American Educational Research Association, builds on an existing body of work on how genetics can contribute to what level of education a person receives. A 2013 study from New York University identified the genetic markers that contribute to a person's level of education, using a pool of 125,000 people from Western Europe, Australia and the U.S.

From those markers, a score referred to as a "polygenic score" is created, estimating just how many years of education a person will complete. But researchers were still unclear on the effects of other factors, like an individual's upbringing, neighborhood and socioeconomic status.

Now, researchers in this new study say that they were able to find a direct cause-and-effect relationship between genetics and educational attainment. And while social factors, like having a parent who has earned a college degree, may have a larger effect on a person's decision to pursue a higher education, genetics can still create a predisposition toward the level of education reached.

Five researchers from colleges throughout the country looked at more than 1,500 siblings in a database known as the National Longitudinal Study of Adolescent to Adult Health. After identifying siblings within the group -- based on the assumption that they would have the same socioeconomic status, parents and neighborhoods -- and comparing their polygenic scores, they found that a sibling with a higher score is more likely to complete more schooling than a sibling with a lower score.

This does not mean that the sibling with the lower score will automatically not reach a higher level of education than the higher-scoring sibling, said Benjamin Domingue, an assistant professor at the Graduate School of Education at Stanford University and a co-author of the paper. He noted that the higher-achieving sibling on average only completed a little less than a third of year of additional schooling compared to the lower achieving sibling.

"It can't be due to being in different environments because they have the same parents, they go to the same schools, they have more or less the same upbringing," said Domingue. "The sibling divide suggests that the genetic relationship is indeed causal."

Domingue said that while the data are new and have to be explored further to effectively apply them in the real world, his findings have implications for the future use of genetics in education. He said policies may be created to make sure that those who may not necessarily be genetically inclined to pursue a higher level of education are still encouraged to do so, and that other factors do still come into play with an individual's decision to complete more years of college.

The paper used a younger group of respondents than past studies that have examined the impact of genetics on education have used. All respondents were in their late 20s or early 30s.

The study also found that with black siblings, the genetic effect was smaller but still significant enough to have an impact. This is the first time that a paper has looked at the genetic impact on level of education attained for the black population.

Domingue said research he and others are working on for a future paper indicates that other factors aligned with success are also associated with pursuing a high level of education -- although it is possible for an individual to achieve success without additional degrees.

"People who are more disposed to get additional years of schooling also have other successes later in life .... This is associated with kind of important things downstream, but more years of education is not the only path to health and stability," he said.

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A new study finds a genetic predisposition to higher levels of education

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A study released today has found that an individual's genetic makeup can have a direct effect on the level of education achieved by that individual, the first time that researchers have found such a relationship. And while the impact is found to be relatively small compared to other external factors, the researchers say it's still significant enough to consider.

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This article shows how genetic researchers have isolated the gene associated with schizophrenia. Considering the complexity of schizophrenia, one must take into consideration the importance of environmental factors, but to know that the basis for the illness is a certain gene, it makes a strong case for the illness to be based in "nature" more than "nuture."

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Researchers have identified a gene that increases the risk of schizophrenia, and they say they have a plausible theory as to how this gene may cause the devastating mental illness.

After conducting studies in both humans and mice, the researchers said this new schizophrenia risk gene, called C4, appears to be involved in eliminating the connections between neurons - a process called "synaptic pruning," which, in humans, happens naturally in the teen years.

It's possible that excessive or inappropriate "pruning" of neural connections could lead to the development of schizophrenia, the researchers speculated. This would explain why schizophrenia symptoms often first appear during the teen years, the researchers said.

Further research is needed to validate the findings, but if the theory holds true, the study would mark one of the first times that researchers have found a biological explanation for the link between certain genes and schizophrenia. It's possible that one day, a new treatment for schizophrenia could be developed based on these findings that would target an underlying cause of the disease, instead of just the symptoms, as current treatments do, the researchers said.

"We're far from having a treatment based on this, but it's exciting to think that one day, we might be able to turn down the pruning process in some individuals and decrease their risk" of developing the condition, Beth Stevens, a neuroscientist who worked on the new study, and an assistant professor of neurology at Boston Children's Hospital, said in a statement.

The study, which also involved researchers at the Broad Institute's Stanley Center for Psychiatric Research at Harvard Medical School, is published today (Jan. 27) in the journal Nature. [ Top 10 Mysteries of the Mind]

Schizophrenia risk
From previous studies, the researchers knew that one of the strongest genetic predictors of people's risk of schizophrenia was found within a region of DNA located on chromosome 6. In the new study, the researchers focused on one of the genes in this region, called complement component 4, or C4, which is known to be involved in the immune system.

Using postmortem human brain samples, the researchers found that variations in the number of copies of the C4 gene that people had, and the length of their gene, could predict how active the gene was in the brain.

The researchers then turned to a genome database, and pulled information about the C4 gene in 28,800 people with schizophrenia, and 36,000 people without the disease, from 22 countries. From the genome data, they estimated people's C4 gene activity.

They found that the higher the levels of C4 activity were, the greater a person's risk of developing schizophrenia was.

The researchers also did experiments in mice, and found that the more C4 activity there was, the more synapses were pruned during brain development.

Molecular cause?
Previous studies found that people with schizophrenia have fewer synapses in certain brain areas than people without the condition. But the new findings "are the first clear evidence for a molecular and cellular mechanism of synaptic loss in schizophrenia," said Jonathan Sebat, chief of the Beyster Center for Molecular Genomics of Neuropsychiatric Diseases at the University of California, San Diego, who was not involved in the study.

Still, Sebat said that the studies in mice are preliminary. These experiments looked for signs of synaptic pruning in the mice but weren't able to directly observe the process occurring. More detailed studies of brain maturation are now needed to validate the findings, Sebat said.

In addition, it remains to be seen whether synaptic pruning could be a target for antipsychotic drugs, but "it's promising," Sebat said. There are drugs in development to activate the part of the immune system in which C4 is involved, Sebat noted.
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"Schizophrenia Gene" Discovery Sheds Light on Possible Cause

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Researchers have identified a gene that increases the risk of schizophrenia, and they say they have a plausible theory as to how this gene may cause the devastating mental illness.

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This article shows that there is a genome that has been proven to be linked to homosexuality in males. While this genome isn't the only thing behind same-sex attraction, there is further research that shows gene presentation during development in the uterus also plays a part.

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For men, new research suggests that clues to sexual orientation may lie not just in the genes, but in the spaces between the DNA, where molecular marks instruct genes when to turn on and off and how strongly to express themselves.

On Thursday, UCLA molecular biologist Tuck C. Ngun reported that in studying the genetic material of 47 pairs of identical male twins, he has identified "epigenetic marks" in nine areas of the human genome that are strongly linked to male homosexuality.

In individuals, said Ngun, the presence of these distinct molecular marks can predict homosexuality with an accuracy of close to 70%.
NEWSLETTER: Get the day's top headlines from Times Editor Davan Maharaj >>
That news, presented at the 2015 meeting of the American Society of Human Genetics on Thursday, may leave the genetically uninitiated scratching their heads.

But experts said the results -- as yet unpublished in a peer-reviewed journal -- offer preliminary new evidence that a man's genetic inheritance is only one influence on his sexual orientation. Through the epigenome, the results suggest, some facet of life experience likely also primes a man for same-sex attraction.

Over a person's lifetime, myriad environmental factors -- nutrition, poverty, a mother's love, education, exposure to toxic chemicals -- all help shape the person he will become.

Researchers working in the young science of epigenetics acknowledge they are unsure just how an individual's epigenome is formed. But they increasingly suspect it is forged, in part, by the stresses and demands of external influences. A set of chemical marks that lies between the genes, the epigenome changes the function of genetic material, turning the human body's roughly 20,000 protein-coding genes on or off in response to the needs of the moment.

While genes rarely change over a lifetime, the epigenome is constantly changing.

Geneticists suggest that together, the human genome and its epigenome reflect the interaction of nature and nurture -- both our fixed inheritance and our bodies' flexible responses to the world -- in making us who we are.

Ngun's study of twins doesn't reveal how or when a male takes on the epigenomic marks that distinguish him as homosexual. Many researchers believe that a person's eventual sexual preferences are shaped in the uterus, by hormonal shifts during key stages of fetal brain development.
FROM THE ARCHIVES: A closer look at scientific inquiry into sexual orientation
By imprinting themselves on the epigenome, though, environmental influences may powerfully affect how an individual's genes express themselves over the course of his life. Ngun's findings suggest they may interact with genes to nudge sexual orientation in one direction or the other.

"The relative contributions of biology versus culture and experience in shaping sexual orientation in humans continues to be debated," said University of Maryland pharmacology professor Margaret M. McCarthy, who was not involved in the current study. "But regardless of when, or even how, these epigenetic changes occur," she added, the new research "demonstrates a biological basis to partner preference."

To find the epigenomic markers of male homosexuality, Ngun, a postdoctoral researcher at UCLA's Geffen School of Medicine, combed through the genetic material of 47 sets of identical male twins. Thirty-seven of those twin sets were pairs in which one was homosexual and the other was heterosexual. In 10 of the pairs studied, both twins identified as homosexual.

In identical twins, DNA is shared and overlaps perfectly. But the existence of twin pairs in which one is homosexual and the other is not offers strong evidence that something other than DNA alone influences sexual orientation. Ngun and his colleagues looked for patterns of DNA methylation -- the chemical process by which the epigenome is encoded -- to identify the missing factor in partner preference.

Their analysis generated a dataset far too large for a team of humans to make sense of. So they unleashed a machine learning algorithm on the data to search for regularities that distinguished the epigenomes of homosexual twin-pairs from twins in which only one was homosexual.

In nine compact regions scattered across the genome, they found patterns of epigenomic differences that would allow a prediction far more accurate than a random guess of an individual's sexual orientation, Ngun reported Thursday.

McCarthy and other experts cautioned that the discovery of epigenomic marks suggestive of homosexuality is a far cry from finding the causes of sexual preference.

The distinctive epigenomic marks observed by Ngun and his colleagues could result from some other biological or lifestyle factor common to homosexual men but unrelated to their sexuality, said University of Utah geneticist Christopher Gregg. They could correlate with homosexuality but have nothing to do with it.

"Epigenetic marks are the consequence of complex interactions between the genetics, development and environment of an individual," said University of Cambridge geneticist Eric Miska. "Simple correlations -- if significant -- of epigenetic marks of an individual with anything from favorite football player to disease risk does not imply a causal relationship or understanding."

One longtime researcher in the field of sexual orientation praised Ngun's use of identical twins as a means of teasing apart the various biological factors that influence the trait.

"Our best guess is that there are genes" that affect a man's sexual orientation "because that's what twin studies suggest," said Northwestern University psychologist J. Michael Bailey, who has explored a range of physiological markers that point to homosexuality's origins in the womb. But the existence of identical twin pairs in which only one is homosexual "conclusively suggest that genes don't explain everything," Bailey added.

While Ngun's research needs to be replicated in larger studies of twins, it advances the fitful process of better understanding how - and when - a boy's sexual orientation develops, Bailey said.

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Scientists find DNA differences between gay men and their straight twin brothers

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For men, new research suggests that clues to sexual orientation may lie not just in the genes, but in the spaces between the DNA, where molecular marks instruct genes when to turn on and off and how strongly to express themselves.

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I believe that most of our traits, habits and personalities are directly related to our genetics, and our individual histories as human beings. Many examples in our society can show that many specific aspects of human beings are innate to our minds, and that these are aspects of our personalities that we cannot decide or control ourselves.